Bclaf1, also known as B-cell lymphoma-2-associated transcription factor 1, was originally identified as a regulator of apoptosis and transcription. It is associated with multiple biological processes such as DNA damage response, pre-mRNA splicing, T-cell activation, lung and muscle development, autophagy, ischemia-reperfusion injury, and viral infection. It is involved in pathways like NF-κB and Hif-1α, and its study via genetic models can provide insights into its functions [1].

In esophageal squamous cell carcinoma (ESCC), Bclaf1 is highly expressed, promoting glycolysis, cell proliferation, invasion, and spread through the YTHDF2-SIX1 pathway [2]. In hepatocellular carcinoma (HCC), it binds SPOP to stabilize PD-L1, facilitating tumor development and immune escape [3]. In lung cancer cells, it induces cisplatin resistance by regulating DNA damage repair and p21-mediated G1 phase arrest [4]. In colorectal cancer, circZFR stabilizes Bclaf1 to promote cancer progression [5]. In bile duct cancer, it may act as an anti-oncogene [6]. In osteoarthritis, Bclaf1 levels are increased in cartilage tissue, and its knockdown in chondrocytes inhibits cartilage degradation [7].

In conclusion, Bclaf1 plays diverse and context-dependent roles in various biological processes and diseases. Studies, including those using gene-knockout or conditional-knockout mouse models (implied by in vivo experiments), have revealed its significance in cancer development, drug resistance, immune escape, and cartilage degradation in osteoarthritis, providing potential therapeutic targets for these disease areas.